rojak Flashcards

1
Q

type 2 pneumocytes produce?

surfactant ___long ass word___ c______

A

surfactant dipalmitoylphosphatidyl choline

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2
Q

cause of plasma exudation???

A

when airway mucosa provoked. airway epithelial cells and endothelial cells exposed to inflammatory mediators (e.g. PAF & histamines), increases permeability, allow for fluid extravasation, macromolecules and cells to escape from blood vessels and into airway walls, interstitial spaces and airway lumen.

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3
Q

cilia description

A
attachments:
apical hools which engage w mucous
cytoskeleton:
9 doublets + 2 central microtubules (axoneme)
nexin links and dynein arms
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4
Q

which part of inspiration and expiration is effort dependent

A

the ENTIRE inspiration dumbass and early expiration

late expiration is effort INdependent like a strong women. amt of air breathed out is the same regardless of effort. depends on compliance and elasticity of lungs and chest wall.

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5
Q

fixed obstruction affect what (flow volume loop)

A

BOTH loops of inspiration and expiration. check notes

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6
Q

variable obstruction got 2 types

  • intrathoracic
  • extrathoracic

each affect what and how (flow volume loop)

A

intrathoracic affect expiratory loop (IE)

  • most severe in expiration, relieved by inspiration
  • due to e.g. excess mucus

extrathoracic affect inspiratory loop (EI)

  • severe in inspiratory, relieved by expiration
  • due to things e.g. tumour
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7
Q

what is dynamic compression, when does it occur

A

forced expiration. intrapleural pressure more positive -> intrapleural pressure > airway (alveolar)
pressure

hence, favour airway compression

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8
Q

to what system/part of brain

voluntary -> ?
reflex->?
emotional->?

A

voluntary -> motor cortex
reflex-> brain stem
emotional -> limbic system

note: locked in syndrome

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9
Q

hemoptysis means what

A

cough blood

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10
Q

HAPE = high altitude pulmonary edema

use what drug

A

nifedipine

which fyi, is also a CCB (calcium channel blocker), which should NOT be used with b-blockers

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11
Q

at which rib does the parietal pleura cross the

  1. midclavicular line
  2. midaxillary line
  3. scapular line

*repeat for lung

A

parietal pleura

  1. 8th rib
  2. 10th rib
  3. 12th rib

lung

  1. 6th rib
  2. 8th rib
  3. 10th rib
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12
Q

isometric contraction vs isotonic contraction

match the feature!

  • isovolumetric ventricular contraction/ventricular ejection
  • no shortening of muscle fibers/shortening of muscle fibers
  • pressure increase, valve close/ enough pressure, valve open
  • associated with preload/afterload (graph)
A

isometric contraction

  • isovolumetric ventricular contraction with NO shortening of muscle fibers. pressure keeps increasing due to exertion by surrounding muscles on chamber with valve close.
  • length tension graph. more preload more force (Frank Starling relationship)

isotonic contraction

  • ventricular ejection, shortening of muscle fibers. once sufficient pressure -> valve open (aortic and pulmonary).
  • graph of muscle shortening against amt of AFTERload experienced. more afterload, less muscle shortening
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13
Q

afterload how to measure

A

use diastolic arterial BP

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14
Q

preload how to measure

A

end diastolic volume + pressure

OR right atrial pressure

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15
Q

calcium bind what in myofilament for contraction

A

troponin c

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16
Q

What pulmonary cell type is primarily involved in connective tissue synthesis?

A

type 2 pneumocytes/epithelial cells

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17
Q

myalgia means what

A

muscle pain

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18
Q

adenocarcinoma. 特点是什么

papillary tumour. 特点是什么

A

adeno -> GLANDULAR structure

papillary -> FINGER-LIKE projections

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19
Q

squamous cell carcinoma 特点是什么

highly associated with what

A

keratinization or intercellular bridges

mutation in tp53 and CDKN2A

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20
Q

Epithelioid histiocytes is what

A

MACROPHAGES

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21
Q

main cellular components of Granulomatous inflammation

A

Epithelioid histiocytes and lymphocytes

note: granulomatous inflammation is the macrophage make a shield around TB

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22
Q

KREBS CYCLE
your almost worst nightmare

citrate to isocitrate what enzyme

A

aconitase dumbass.

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23
Q

kreb cycle

ENZYMESSSSSSSS

oxaloacetate -> citrate -> isocitrate -> a-ketoglutarate -> succincyl coa -> succinate-> fumarate -> malate -> oxaloacetate

A
  1. acetyl coa
  2. aconitase
  3. isocitrate dhg
  4. a-ketoglutarate dhg
  5. succinyl coa synthase
  6. succinate dgh
  7. fumarase
  8. malate dgh
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24
Q

alternaria is what and cause what

A

plant pathogen. cause allergic rhinitis

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25
Q

which pathway of the 3 allergic thing is just built different

  1. allergic rhinitis
  2. asthma
  3. allergic alveolitis
A

allergic alveolitis is non IgE mediated while the rest are IgE mediated

allergic alveolitis is IgG mediated

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26
Q

C3a and C5a do what

A

CHEMOKINES so they CHEMOTAXIS. they activated by proteases then increase inflammation by yelling at the cells that the bacteria is here. aka the modern billboards

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27
Q

classical pathway of complement system is how

A

1 4 2 3b 5b 6 7 8 9

5b 6 7 8 9 break off form MAC
3b used for opsonisation, bind to macrophage through C3b receptor

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28
Q

C5a C6 C7 C8 C9 make what for what

A

MAC = membrane attack complex

they attack the bacteria membrane and make a hole so the enzyme and shits can enter the bacteria. so the bacteria die bad bad

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29
Q

alternative pathway how

A

C3b directly bind, then the rest same same as classical pathway

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30
Q

lectin pathway (complement system) is what

A

C4 bind to mamose. then just continue from there.
c4 c2 c3b 5b 6 7 8 9
then same same

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31
Q

pyrexia means what

A

fever

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32
Q

Where is the breast located?

  1. what region?
  2. where does it extend from?
A

situated in superficial fascia of the pectoral region.

extend vertically from the 2nd to the 6th rib in the midclavicular line.
extends horizontally from lateral border of the sternum to the midaxillary line at the level of 4th costal cartilage

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33
Q

retromammary space is what

A

space that separates the breast from the pectoral fascia (and muscles)

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34
Q

retromammary space got what, for what

A

loose areolar tissue, allow for free movement of the breast on these muscles

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35
Q

areolar tissue got what, for what

A

loose connective tissue composed of collagen, elastic fibres and reticular fibres

for: bind skin to muscles beneath, provide support, strength and elasticity to the tissues

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36
Q

mammary gland got what

A

mammary gland tissue, fibrofatty tissue, connective tissue, blood vessels and lymphatics

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37
Q

lactiferous duct do what

A

drain each lobule, opens independently into top of nipple

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38
Q

breast blood drains into? (3 veins)

A

internal thoracic vein, axillary vein (mainly) and intercostal veins, along intercostal neurovascular bundle

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39
Q

suspensory ligaments? (breast)

A

connective tissue between gland lobules. extend from skin to pectoral fascia.

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40
Q

4 quadrants of the breast?

A
A. upper outer quadrant (superolateral)
B. upper inner (superomedial)
C. lower inner (inferomedial)
D. lower outer (inferolateral)
A | B
-----
C | D
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41
Q

chromosomal mis-segregration occur which stage of mitosis

A

metaphase

note: checkpoint kinase inhibitors are used in anti-cancer therapy => inhibit spindle assembly checkpoint @metaphase

inhibitor e.g. Taxane, cause premature mitosis, chromosomal mis-segregation and apoptosis

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42
Q

why RBC tend to burst aka lyse in low tonicity/ why WBC got more resistance

A

RBC no ATP bro. no energy unlike WBC. cannot transport Na+ out of cell which controls the water potential remember???

Na+/K channel is the osmolarity controller

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43
Q

hydrostatic pressure vs colloid pressure which direction

A

google it. but to describe:

colloid is outside vessel to inside
hydrostatic is inside vessel to outside vessel

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44
Q

tonicity vs osmolarity

A

osmolarity takes into account the total concentration of penetrating solutes and non-penetrating solutes, whereas tonicity takes into account the total concentration of non-freely penetrating solutes only.

tldr: tonicity care about semi-permeable membrane

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45
Q

what is SLE

A

Systemic lupus erythematosus. immune system attacks its own tissues, causing widespread inflammation and tissue damage in the affected organs. It can affect the joints, skin, brain, lungs, kidneys, and blood vessels.

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46
Q

what are the 7 oncoviruses?

A

hep B, hep C, human T lymphotropic virus, merkel cell polyomavirus, human papillomavirus, Epstein Barr virus, HHV-8

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47
Q

what are the associated cancers for the 7 oncovirus?

hep b, hep c, human t lymphotropic virus, merkel cell polyomavirus, HPV, HHV-8, Epstein-Barr

A

hep b -> hepatocellular carcinoma
hep c -> hepatocellular carcinoma
human t lymphotropic virus (HTLV) -> adult T cell leukaemia
merkel cell polyomavirus -> merkel cell carcinoma
ebstein barr virus -> burkitt’s lymphoma, hodgkin’s lymphoma
HHV-8 -> kaposi’s sarcoma
human papillomavirus -> cervical cancer, anal cancer, etc,

!!! hep c and HTLV RNA virus , the rest DNA

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48
Q

RAS pathway. what are the steps

A

peptide growth factors -> tyrosine kinase receptors -> receptor dimerise and cross phosphorylate -> recruit adaptor and signaling protein Grb2 + Sos (protein/exchange factor) -> RAS GTP binding protein activated -> exchange of GDP for GTP -> active (bound to plasma membrane) Ras protein -> activate protein kinase cascade

protein kinase cascade:
activated kinase 1 [RAF, MAPKKK] use gamma phosphate in ATP phosphorylate kinase 2 [MEK, MAPKK] -> kinase 2 use ATP phosphorylate kinase 3 [ERK, MAPK]

MAPK: mitogen-activated protein kinase

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49
Q

Herceptin is what

A

anti-HER2 antibody. block the HER2 receptor tyrosine kinase

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50
Q

cyclin dependent kinases (CDK) at M, G and S phase

A

M phase: cdk1 + cyclin B = m-cdk (MPF= m-phase promoting factor)
G phase: cdk2 + cyclin E = G1/S-cdk
S phase: cdk2 + cyclin A = S-cdk

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51
Q

whats the point of ERK

A

ERK phosphorylates and upregulate expression of Myc to express cyclin D. cyclin D bind to cdk4/6 and Rb protein to release E2F transcription factor

cyclin E transcribed -> bind to cdk2 -> drive G1 to S phase

cdk2-cyclinE phosphorylate Rb -> release more E2F -> transcribe cyclin A

cyclin A -> bind to cdk2 -> enter S phase

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52
Q

rice water stools means kena what

A

cholera

^ will have increased cAMP cause Cl- EFflux into gut lumen
note: usually presented with no blood in faeces.
cholera presents with large volume losses -> fluid loss, electrolyte loss

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53
Q

watery diarrhoea means what

what can cause it

A

non invasive, increased secretion of water and electrolytes

causes:
bacteria - vibrio cholerae, ETEC (E. coli), S. aureus
virus - norovirus, rotavirus
parasite- giardia duodenalis aka giardia intestinalis/lamblia (the parasite look like face LOL)

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54
Q

bloody diarrhoea means what

caused by what

A

invasive; pathogenesis includes toxins that kill enterocytes

causes:
bacteria- shigella dysenteriae, EHEC (E. coli), Salmonella spp, Campylobacter jejuni (curved, look like w)
parasites- entamoeba histolytica

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55
Q

complication of cholera

A

hypokalemic metabolic acidosis

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56
Q

CD8+ T cell recognize what type of antigen (exogenous or endogenous) on what MHC

A

endogenous on MHC1

cd8 are your cytotoxic!!! they release the granzymes and perforin so then the cell so poof. they kill those 不是自己人

T cells cells diff: T cells recognise exogenous on MHC2!!

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57
Q

to inhibit Treg to reduce immunosuppression

A

anti CTLA-4 antibody: ipilimumab, tremelimumab
^ downregulation of out competition of CD28 binding to B7 (inhibits T cells)

anti PD-1 antibody: nivolumab, pembrolizumab
anti PD-L1 antibody: MPDL3280A
^ downregulation of PD-1 (Effector T cell) and PD-L1 (Treg/tumour cell) binding

therefore, more T cell, higher immuno :D

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58
Q

Beri-beri caused by what

A

deficiency of vitamin B1

problem with TPP (pyruvate dehydrogenase complex)

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59
Q

beta oxidation what 4 steps.

what do u get in the first step of b-oxidation

A

OHOT

oxidation, hydration, oxidation and thyolisis (aka cleavage)

first step: acyl CoA
last step: 2 acetyl CoA

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60
Q

what are some tumour suppressor genes?

A

p53, bRCA1, PTEN, APC, p16 INK4a, MLH1

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61
Q

function, location and associated cancer of the tumour suppressor genes

p53, BRCA1, PTEN, APC, p16 ink4A, MLH1

A

p53 -> cell cycle regulator, nuclear, many e.g. colon, breast, bladder, lung
BRCA1 -> cell cycle regulator, nuclear, breast & ovarian & prostate
PTEN -> tyrosine and lipid phosphatase, cytoplasmic, prostate & glioblastoma
APC -> cell signaling, cytoplasmic, colon
p16ink4A-> cell cycle regulator, nuclear, colon and others
MLH1 -> mismatch repair, nuclear, colon and gastric

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62
Q

initiator caspases that trigger cell death programme (apoptosis)

effector caspases that carry out later stages of cell death (apoptosis)

A

initiator: caspase 2, caspase 9, caspase 10, caspase 8
effector: caspase 3, 6, 7

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63
Q

four hypersensitivity types

A

Type I: reaction mediated by IgE antibodies.
* allergic rhinitis. degranulation of mast cells, release of histamine, asthma

Type II: cytotoxic reaction mediated by IgG or IgM antibodies.
*Graves disease, overactivated thyroid! not thymus! THYROID. autoimmune disease

Type III: reaction mediated by immune complexes.
*Rheumatoid arthritis, SLE

Type IV: delayed reaction mediated by cellular response.
*poison ivy rash, Rheumatoid arthritis

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64
Q

allergic asthma is what type of INFLAMMATION

**not hypersensitivity

A

type 1/4

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65
Q

graves disease, rheumatoid arthritis, poison ivy what type of hypersensitivity

A

graves disease-> type 2
rheumatoid arthritis-> type 3
poison ivy rash -> type 4

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66
Q

DiGeorge syndrome is what

A

highest concentration of IgM, have hypoplastic/absent thymus. T cell cannot mature, therefore no class switching to B cell. therefore, only IgM produced

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67
Q

what type of necrosis associated with acute pancreatitis

A

fat necrosis.

pancreatic lipase leak out of pancreas to digest fat in the abdomen. fatty acids produced can combine with calcium to form visible chalky deposits

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68
Q
what are 
1. coagulative necrosis
2. caseating necrosis 
3. fibrinoid necrosis 
4, liquefactive necrosis
5. fat necrosis  
associated with
A
  1. infarction in solid organs, other than the brain e.g. myocardial infarction
    * proteins denature -> form gelatinous substance -> maintain tissue architechture
  2. tuberculosis, looks like cheese
    * dead cells disintegrate but no completely digested -> soft, white proteinaceous mass of granular debris walled off by a distinctive inflammatory border (grannuloma)
  3. deposition of antigen-antigen complexes within blood vessel
  4. hypoxic infarcts in BRAIN
    * dead cells digested by own enzymes -> viscous, liquid mass in cystic space (abscess formation)
  5. acute pancreatitis
    * activated lipase necrose fat tissue -> lesion can bind calcium to product soap/ calcium deposits
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69
Q

atrial fibrillation complication

A

cerebrovascular attack.

AF due to to arrhythmias cause stasis, create thrombus in left atrium. then reach brain where occludes (stroke)

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70
Q

characteristics of DVT:

____in extremities. ____ lodge within pulmonary artery -> cause _____ -> cause ____-> cause _____ since heart try to pump harder

A

varicosities in extremities. thrombus lodge within pulmonary artery -> cause pulmonary embolism -> cause pulmonary hypertension -> cause right ventricular failure since heart try to pump harder

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71
Q

lobar pneumonia caused by what

A

usually bacterial infection.

less common: viral/fungal

treatment: antimicrobial therapy

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72
Q

which pneumonia associated with

  1. haemophilus influenza
  2. staph aureus
  3. strep cocci/pneumococci
  4. TB
  5. pneumocytis jiroveci
  6. aspergillus
  7. influenza, adenovirus, varicella
A
  1. bronchopneumonia
    * virus, has fimbriae, hair-like structure to anchor on airway epithelial cells to prevent removal by mucociliary clearance
  2. bronchopneumonia
  3. bronchopneumonia and lobar pneumonia
  4. bronchopneumonia
  5. interstitial pneumonia
    * fungi, usually in severely immune suppressed individuals
  6. interstitial pneumonia
  7. interstitial pneumonia
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73
Q

bronchiectasis is what, symptoms got what

bronchiectasis vs bronchitis

A

bronchiectasis: chronic, necrotising infective inflammatory condition => permanent irreversible dilatation of airways
bronchitis: inflammation of mucous membrane in bronchi

symptoms:
bronchiectasis - green/brown/blood-stained sputum (blood due to necrosis and infection), chocolate brown material in bronchiole wall since decreased elastin
bronchitis - white to yellow mucous, only if super infected then green to brown mucous, less sputum than bronchiectasis

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74
Q

root of right lung (hilum) posterior anterior got what

A

posterior: azygous vein
anterior: SVC

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75
Q

thoracic aortic aneurysm can lead to compression of what

A

thoracic duct and oesophagus

note: thoracic duct ascend through aortic hiatus, right of the aorta and cross to the left (posterior to oesophagus at T5)

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76
Q

use of accessory muscles for inspiration implies what

A

inability to use diaphragm (cannot contract) and thus, phrenic nerve injury => raised hemidiaphragm

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77
Q

phrenic nerve supply what

A

fibrous pericardium, diaphragmatic peritoneum, parietal pleura,

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78
Q

kussmaul respiration is what

A

deep, regular sighing breaths with any rate, represent respiratory compensation for metabolic acidosis (low bicarbonate)

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79
Q

women go mountain, lung how change

A

high altitude -> low o2 level -> HPV -> increased pulmonary resistance

due to low pAo2 -> alveolar ventilation -> reduction of PaCO2, increase pH, o2 curve shift left (respiratory alkalosis)

compensation:
respiratory alkalosis - renal compensation -> alveolar ventilation -> pao2 rise -> pH return

o2 curve shift left - RBC glycolysis -> increased production of 2,3-DPG, binds allosteric site of globin chain -> stabilize low affinity state -> shift o2 curve to RIGHT (facilitate tissue unloading)

increased hematocrit (no. of RBC) since lesser o2, stroke volume = CO x TPR and heart rate increase

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80
Q

pink frothy sputum means what

A

pulmonary oedema: will have impaired gas exchange, reduced lung compliance, increased pulmonary venous pressure

other symptoms: terrified, severe SOB, crackles heard upon auscultation (since inspiration opens alveoli with fluid)

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81
Q

o2 curve shift left vs right

A

left: loading of o2 (higher affinity of hb)
right: unloading of o2 (lower affinity of hb)

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82
Q

causes for o2 curve shift left

+ where

A

left:
increased pH (alkalosis)
reduced PaCO2 (bohr effect)
reduced body temp

foetal Hb, pulmonary capillaries

note: shift right just switch opposite
- maternal hb, and stored blood (detrimental), metabolically active tissue (unload o2)

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83
Q

sleep vs awake

A

when awake, tidal volume increases!! more respiratory muscles used when breathing (more effort)

other effects! but less
alveolar ventilation increases (increased respiratory effort)
SaO2 of arterial blood increases slightly
PaCo2 of venous blood decreased (body doesnt reach apnoeic threshold before stimulation of breathing)
breathing rate increases

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84
Q

stroke volume or Pao2 reduction by 20% more jialat

A

stoke volume reduction

!! only 2% of o2 transported in blood is in PaO2, 98% bound to Hb.
!!! 20% drop of SV means 20% drop of o2 delivery

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85
Q

contraction of diaphragm during inspiration or expiration

A

EXPIRATION BODOH

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86
Q

how to expire at super fast speed zoom zoom

A

breath in larger initial volume before breathing out

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87
Q

how much blood loss and what class

HR <100, BP and PP normal, RR 14-20
UOP >30, CNS slightly anxious

A

class 1, <740ml ~15% blood loss

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88
Q

how much blood loss and what class

HR >100, BP normal, PP decrease, RR 20-30
UOP 20-30, CNS madly anxious

A

class 2, 750ml-1500ml 15%-30% blood loss

note: normal blood ~5000ml

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89
Q

how much blood loss and what class

HR >120, BP and PP decrease, RR 30-40
UOP 5-15, CNS anxious confused

A

class 3, 1500-2000ml 30-40% blood loss

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90
Q

how much blood loss and what class

HR >140, BP and PP decrease, RR >35
UOP negligible, CNS confused and lethargic

A

class 4 >2000ml >40% blood loss

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91
Q

RAA system describe

A

angiotensinogen -> angiotensin 1 (enzyme: renine)
angiotensin 1 -> angiotensin 2 (enzyme: ACE)

bradykinin decrease -> NO decrease -> vasoconstriction
AT2 bind to AT1 -receptor -> release aldosterone -> retain SODIUM

OVERALL EFFECT: INCREASED BLOOD PRESSURE

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92
Q

types of shock (4 types)

A

hypovolaemic, cardiogenic, distributive, obstructive

note: 
distributive
* septic shock, anaphylactic shock 
cardiogenic
* dysfunction of heart muscle, inability to pump and supply blood to organs
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93
Q

anterior infarct which lead have ST elevation

A

V1, V2, V3 and V4

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94
Q

which lead ST elevation for lateral infarct

A

lead I, V5, V6, aVL

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95
Q

Von Willebrand disease is what

A

primary haemostatic disease.

epistaxis, prolonged gum bleed, menorrhagia (menstruation longer than 7 days), easy bruising

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96
Q

Von Gierke’s disease is what

A

2 mutant copies of G6Pase (glucose-6-phosphatase) gene inherited. one from each parent -> G6Pase deficiency

characteristics -> low blood sugar, slow growth, large livers, short stature

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97
Q

Von Gierke’s disease is what

A

2 mutant copies of G6Pase gene inherited. one from each parent -> G6Pase deficiency

characteristics -> low blood sugar, slow growth, large livers, short stature

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98
Q

Barrett’s esophagus is what

A

metaplasia!!

non-keratinised stratified epithelial cells replaced by simple columnar epithelial cells when exposed to stomach acid (E.G. during stomach acid reflux)

note: metaplasia is reversible!!

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99
Q

anomaly during metaphase -> daughter cells have unequal amount of DNA

A

deficiencies in BUB kinase signaling

  • BUB kinase generate checkpoint signals during metaphase when kinetochores are not bound to microtubules
  • prevent anaphase from taking place until all kinetochore attached to MT
  • deficiency = premature anaphase
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100
Q

amphitelic attachment of microtubule to chromosome kinetochore normal anot

A

yes. amphitelic literally means proper attachment of spindle attachment

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101
Q

abberrant cytokinesis -> unequal amount of DNA occurs when

A

cytokinesis AFTER mitosis

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102
Q

transcription of DNA occur which direction

A

5’ to 3’

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103
Q

binding of elF2 to GTP and Met-tRNA involved in what process

A

translation!!

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104
Q

what is profilin

A

profilin = protein assist microfilament elongation

*exchanges ADP for ATP on actin monomers -> convert to readily polymerizing form

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105
Q

how does polymerisation of MT occur

A

nucleation: require tubulin, Mg, GTP, 37 degrees. SLOW
elongation: polymerisation of dimer, happens at PLUS END if GTP present
note: MT does not keep growing if GDP is at the plus end

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106
Q

5 types of intermediate filament

A

type 1 and 2: acidic keratin (type 1) and basic keratin (type 2)
* found in epithelial cells (bladder, skin, etc)

type 3: cell types include

  • vimentin (fibroblasts, endothelial cells, leukocytes)
  • desmins (desmosomes e.g. cardiac muscle, skeletal muscle)
  • glial fibrillary acidic protein GFAP (in astrocytes)
  • peripherin (peripheral nerve fibers)

type 4: neurofilament

  • heavy, medium, low
  • modifiers refer to molecular weight of protein, mainly in axonal cells

type 5: lamins

  • filamentous support inside inner nuclear membrane
  • vital for reformation of nuclear envelope after cell division
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107
Q

what does gelsolin do to microfilament aka actin

A

gelsolin binds to +end!

gelsolin involved in severing and capping microfilament -> increase number of filaments avail -> increase TOTAL RATE of elongation

note:
ARP 2/3 and WASP assist in nucleation of microfilament
filamin assist microfilament bundling

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108
Q

prokaryote DNA replication how many origin

A

ONLY ONE. remember its a CIRCLE!! so only form ONE replication bubble

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109
Q

reduced protein in interstitium, pressure how

increased protein in capillaries, pressure how

A
  1. (reduced protein, interstitium) interstitial colloid osmotic pressure decreases
    note: therefore, less water pulled into of interstitium, into the blood vessel.

INCREASED circulatory volume
2. (increased protein, capillaries) plasma colloid osmotic pressure increase, retain fluid in plasma

110
Q

wtf are schwann cells

A

main glial cells of the peripheral nervous system which wrap around axons of motor and sensory neurons to form the myelin sheath.

tldr: MYELIN SHEATH `

111
Q

schwann cell do what

A

allow for myelination -> allow for high AP conduction velocity 150m/s due to saltatory conduction

note: unmyelinated only 0.5-10m/s only

112
Q

excess acetylcholine do what to your sweat

A

INCREASE production!! sweat glands stimulated by secretion of acetylcholine

113
Q

organ abscess caused by what

clue: entamoeba

A

entamoeba migration to organs through bloodstream after penetrating enteric mucosa

114
Q

acute exacerbation of asthma use

  1. short acting muscarinic agonist or antagonist to treat
  2. long acting beta-adrenergic antagonists or agonist to alleviate bronchial smooth muscle constriction
A
  1. ANTAGONIST!! we want to block PARAsympathetic pathways to lungs -> inhibition of bronchoconstriction
  2. agonist!! initiate sympathetic -> bronchodilation
115
Q

dropping eyelids, constricted pupil, dryness of face on right side is what syndrome

A

right sided Horner’s syndrome

* arises from lesion of sympathetic chain at T1/T2

116
Q

localised cholecystitis (redness and swelling of gallbladder) affect what

A

greater splanchnic nerve

symptom: right upper quadrant pain

117
Q

axillary artery

  1. branch of what artery
  2. supply what
A

subclavian artery. supply axilla and upper limb

118
Q

which organism NOT causative agent of IE

  1. eikenella corrodens
  2. acinetobacter baumannii
  3. viridans streptococcus
  4. aggregatibacter actinomycetemcomitans
A

acinetobacter baumannii

119
Q

b1, b2-receptor where

A

b1-> on heart, facilitate sympathetic activation @SA node

b2-> in lungs

120
Q

what condition or mechanism failure cause syncope (fainting)

A

lack of a1 adrenoceptor stimulation.

syncope -> hypotension, lack of perfusion to brain
^ caused by insufficient CO increase/insufficient peripheral vascular resistance

MAP = CO x TPR

note:
a1 adrenoreceptor found on PERIpheral blood vessels -> activated for vasoconstriction
b2 adrenoreceptor found on blood vessels -> activated for vasodilation -> decrease BP
hypotension decrease baroreceptor stimulation

121
Q

lowered pH caused by ketone bodies detected by?

A

chemoreceptors

122
Q

baroreceptor describe

  1. via what
  2. effects if increase
  3. where
A

via vagus nerve. if increase baroreceptor firing, INCREASE parasymp, DECREASE symp, DECREASED HR

at aortic arch and carotid sinus

stimulated by arterial pressure drop (BP drop)

note: to test, use valsava
* increased intrathoracic pressure, decreased venous return, decreased cardiac output, therefore, DECREASE IN ARTERIOLE PRESSURE, parasymp increase, symp decrease, HR increase

123
Q

what affects sensitivity of baroreceptors

A

chronic hypertension

124
Q

peripheral and central chemoreceptors

  1. where
  2. respond to what
A

peripheral

  1. aortic arch & carotid bodies
  2. hypoxic (low PaO2), high PaCO2, low blood pH

central

  1. surface of medulla
  2. KETONE BODIES, high PaCO2, low pH in cerebrospinal fluid
125
Q

b1, b2-receptor where

A

b1-> on heart, facilitate sympathetic activation @SA node

b2-> in lungs

126
Q

smokers! bronchus! got increased density of blood vessel?

A

YES!

note: there will be a proliferation of smooth muscle myocytes as well!

127
Q

oedema cause in MALNOURISHED

A

malnourish-> proteolysis (to generate aa for metabolism for energy) -> decreased serum albumin levels -> DECREASE COLLOID OSMOSTIC PRESSURE (aka low blood protein level) -> oedema

128
Q

multiple sclerosis how affect neuron

A

autoimmune disease where Schwann cells are attacked. therefore reduce speed of conductance of neuron

129
Q

multiple sclerosis how affect neuron

A

autoimmune disease where Schwann cells are attacked. therefore reduce speed of conductance of neuron

130
Q

anti CTLA-4 antibody mechanism

A

upregulate activation of naive T cells by dendritic cells

note: anti CTLA-4 antibodies used as checkpoint therapy against cancer

CTLA-4 found on naive T cell soon after activation
CTLA + B7 (on dendritic) binding downregulate activation of T cell
***CTLA-4 expressed on Treg = downregulate ability of dendritic cells to present antigen

131
Q

pulmonary surfactant first formation in baby (how many weeks, which period)

when does surfactant-secreting type 2 pneumocytes differentiate the most (what period)

A

terminal saccular period

132
Q

key difference between COX-1 and COX-2

A

COX-1 found in healthy individuals

COX-2 switched on during inflammation and pain

133
Q

RNA polymerase I, II and III used for what type of RNA

A

I: rRNA
II: mRNA
III: tRNA and 5S RNA

134
Q

tamoxifen for what

A

breast cancer. block estrogen receptor

135
Q

anticodon that tRNA delivers methionine?

A

CAU (5’-3’)

REMEMBER DIRECTION

136
Q

does translation use GTP/ATP and what enzyme

A

GTP + peptidyl transferase

137
Q

translation: preinitiation complex involve binding to what subunit

A

60S subunit

  1. Dissociation of ribosome into 40S + 60S subunit
  2. Assembly of preinitiation complex
    * Met- tRNA (since start codon is always AUG)
    * eIFs (eukaryote initiation factor)
    * 40S subunit
  3. Binding of mRNA to preinitiation complex
  4. Binding of 60S subunit
138
Q

what do the following meds act on what in bacteria

  1. streptomycin
  2. tetracyclin
  3. erthromycin
  4. chloramphenicol
  5. puromycin
A
  1. streptomycin - inhibit initiation
  2. tetracyclin - inhibit aa-tra binding
  3. erthromycin - inhibit translocation of ribosome along mRNA
  4. chloramphenicol - inhibits peptidyl transferase
  5. puromycin - terminates elongation prematurely
139
Q
CARCINOGENESIS
effect  and source of 
1. benzo [a] pyrene
2. aflatoxin B2 from Aspergillus flavus mold 
3. 2-napthylamine 
4. pyrimidine (thymine dimers)
5. free radicals
A
  1. benzo [a] pyrene
    * DNA adducts, pollutants
  2. aflatoxin B2 from Aspergillus flavus mold
    * liver carcinogen, poorly stored grains and peanuts
  3. 2-napthylamine
    * bladder cancer, dye-industry
  4. pyrimidine (thymine dimers)
    * skin cancer, solar radiation
  5. free radicals
    * strand breaks, base modifications, ionising radiation
140
Q

hybridisation stringency increases with?

A

higher temp and DECREASE in Na+ conc

note: at high stringency, only DNA sequences which are EXACTLY identical will bind

141
Q

which end does elongation of MT occur preferentially?

A

plus end

142
Q

MT associated proteins bind to MT for?

A
  1. to stabilize them
  2. to cross-link them
  3. attach them to other cellular components: membranes, intermediate filaments, other MT
143
Q

actin: got 2 types, what are they

A

G-actin (globular) - actin monomers
*ATP bind w actin monomers = ATP hydrolysed => ADP-actin and Pi
F-actin (filamentous) - actin filaments

144
Q

Cellular poisons against actin filaments

A

!! active at low concentration

  1. cytochalasin - inihibit polyermerisation/depolymerisation
  2. latrunculin - inhibit polymerisation
  3. phalloidin - binds to and stabilise F-actin
145
Q

capping proteins, 2 types :
+end and -end

name some examples

A

+end: cap z, gelsolin, fragmin/severin

-end: tropomodulin, arp complex

146
Q

filopodia is what

A

tight parallel bundles

note: formation by actin polymerisation, bundling and cross-linking
note: stress fibre creates tension and facilitates retraction of cell

147
Q

profilin vs thymosin

A

profilin help to take the G-actin to F-actin: yay! polymerisation!!
thymosin block the G-acting, kidnapping!: OH NO! no polymerisation

148
Q

lamellipodia

A

sheet like protrusion

note: formation facilitated by arp2/3 complex (branching) and cofilin (disassembly)
note: stress fibre creates tension and facilitates retraction of cell

149
Q

intracellular protein transport 3 types

A
  1. gated transport
  2. protein translocation
  3. vesicular transport
150
Q

various coat proteins that involve in shaping vesicles include?

A

COPI, COPII, Clathrin

151
Q

Marfan Syndrom

A

Fibrillin 1 mutation

  • predispose aortic rupture
  • elastic fibre
152
Q

Osteoarthritis due to what

A

loss of ECM (degenerative disease), due to cleavage and loss and aggrecans

153
Q

cystic fibrosis

A

CFTR gene, degradation of transmembrane receptor

154
Q

intermediate mesoderm become what

A

kidney, gonads, adrenal cortex

155
Q

heart nerve fibres & area of referred pain

A

T1-5

left precordium n left upper limb

156
Q

stomach nerve fibres n area of referred pain

A

T5-9

lower chest n abdominal wall

157
Q

gallbladder nerve fibres

A

T5-9,
lower chest and abdominal wall

note:
if infection spread to peripheral diaphragm and anterior abdominal wall
*6th-11th ics nerves, R upper quadrant of abdominal wall, all the way to inferior angle of scapula

if infection spread to CENTRAL diaphragm
*C3-C5, right shoulder

158
Q

posterior parietal cortex required for what, associated with what syndrome

A

required for attention!!!
associated with hemispatial neglect syndrome if damaged.

note: hemispatial neglect syndrome = when asked to draw clock, left blank but right half filled

159
Q

what do the following metabolic poisons do

  1. rotenone
  2. malonate
  3. cyanide and azide
  4. carbon monoxide
  5. oligomycin
  6. dinitrophenol and thermogenin/UCP-1
  7. arsenite and mercury
A
  1. rotenone - inhibit NADH dhg
  2. malonate - competitive inhibitor of succinate dhg
  3. cyanide and azide - bind to ferric (Fe3+) in cytochrome oxidase
  4. carbon monoxide - bind to ferrous (Fe2+) in cytochrome oxidase
  5. oligomycin - binds to stalk region in ATP synthase
  6. dinitrophenol and thermogenin/UCP-1 - decoupling of ATP synthase
  7. arsenite and mercury - readily inhibits pyruvate dhg
160
Q

tissue distribution of hexokinase I and glucokinase (aka hexokinase IV)

A

hexokinase I: skeletal muscles

glucokinase aka hexokinase IV: liver cells (hepatocytes), pancreas B cells

161
Q

hexokinase I vs glucokinase (aka hexokinase IV)

  1. glucose affinity
  2. regulation
A
  1. glucose affinity

hexokinase:
high glucose affinity (LOWER Km),
effective at LOW conc. ineffective at high conc
LOWER binding capacity (LOWER Vmax)

glucokinase:
LOW glucose affinity (HIGHER Km)
effective at HIGH conc, ineffective at low conc
HIGHER binding capacity (higher Vmax)

  1. regulation

hexokinase:
allosteric inhibition by G6P

glucokinase:
inhibition by glucagon
*less sensitive to G6P inhibition
activated by insulin

162
Q

creatine phosphate importance?

process catalyzed by?

A

source of ATP in muscles, buffer demands for ATP during intense exercise

catalyzed by creatine kinase

note: if muscle is damaged, creatine kinase leaks into bloodstream
!!!!creatine KINASE useful diagnostic marker for muscle injuries
*(can be used to diagnose/evaluate/discover)
elevated = MI, extent of muscular disease, chest pain, carrier of muscular dystrophy [duchenne]

163
Q

embryology

what week to what week

  1. pseudoglandular period
  2. canalicular period
  3. terminal saccular period
  4. alveolar period
A
  1. week 5-17
  2. week 16-27
  3. week 24-38
  4. week 36-8 years
164
Q

end systolic volume determined by closure of what valve

A

aorticcc

165
Q

brain reliant on what metabolism

A

GLUCOSEEE!!

cannot use b-oxidation of fat in brain!

166
Q

net yield of krebs cycle

A

6NADH, 2GTP, 2FADH, 4CO2
^for one GLUCOSE not one cycle

note: energy yield 24 ATP
* 6 x3 + 2x2 + 2x2 =24

167
Q

which is the SOLE insoluble protein in mitochondrial matrix

A

succinate dehydrogenase

*found on inner mito membrane

168
Q

NADH transport from cytosol to inside mito matrix how (2 shuttles)

A

glycerol-phosphate & malate aspartate

169
Q

glycerol phosphate vs malate aspartate

  1. found where
  2. atp yield per nadh
  3. pass electron to
A

note: shuttles above transport NADH from cytosol into mito matrix

  1. found where
    glycerol phosphate- skeletal muscle and brain
    malate aspartate - liver, kidney and heart
  2. atp yield per nadh
    gly phos - 1.5
    mal asp - 2.5
  3. pass electron to
    gly phos - FADH2 (skips etc 1)
    mal asp - NADH
170
Q

describe how gly-pho shuttle works

A

cytosol glycerol-3-phosphate dhg
*transfer electron from nadh to glyercol-3-phosphate

then mitochondrial glycerol-3-phosphate
*electron transferred to FAD -> then passed to co-enzyme Q (ETC)

171
Q

ETC describe
electron move from what order
how many complex and mobile carrier

A
NADH dhg (NADH) or succinate dhg (FADH2) -> ubiquinone (co-enzyme Q) -> cytochrome b-cl -> cytochrome c -> cytochrome oxidase
with o2 as the terminal electron acceptor 

3 complexes, 2 mobile carriers

172
Q

atp synthase structure describe

A

F1 (part projecting into matrix)
- A, B, Y subunit
F0 (membrane bound part)
- abc subunit

note:
c and Y rotate
a, b, A, B do not rotate
A, B change conformation to generate ATP

watch youtube video to visualise mechanism!

173
Q

5 reactions of gluconeogenesis (what catalyst)
1. pyruvate -> oxaloactetate

  1. oxaloacetate -> phosphoenolpyruvate
  2. fructose-1,6-biphosphate-> fructose-6 phosphate
  3. fructose-6 phosphate -> glucose-6-phosphate
  4. glucose-6-phosphate -> glucose
A
  1. pyruvate carboxylase
    *allosterically activated by acetyl-coa
    (break down too much glucose -> make more glucose)
  2. phosphoenolpyruvate carboxykinase
  3. fructose-1,6-biphosphatase
  4. phosphoglucoisomerase
  5. glucose-6-phosphatase (
174
Q
b-oxidation, 
how much ATP from 
1 acetyl coa 
1 fadh2
1 nadh
A

acetyl coa -> TWELVE 12 SHI ER!!
fadh2-> 2
nadh -> 3

175
Q

how to find out how many b-oxidation cycle it need to go through

and how many acetyl coa

A

b-oxidation cycles: (no. of carbon of fatty acid - 2) / 2

acetyl coa: no. of carbon fatty acid/2

176
Q

4 steps of lipogenesis (fat acid synthesis) on top of the transference of carbon groups to acyl carrier protein (ACP)

  • 1 malonyl-acp (3c)/cycle
  • 1 acetyl-acp (2c)
A

CRDR
condensation, reduction, dehydration, reduction
(2NADPH used)
^ OI GOT A P CUZ THIS IS SYNTHESIS NOT DEGRADATION OK
rmb SymPathetic

177
Q

MCADD
medium chain acyl coenzyme a dhg deficiency
treatment?

A

treatment:

  1. never go w/o food more than 10-12 hours
  2. high carbs diet
  3. IV glucose if cannot consume glucose (vomiting)
    * note: autosomal recessive

pt unable to oxidase fats as energy source

178
Q

cholesterol synthesis molecule steps

A

Mevalonate (C6) -> Isopentyl (C5) -> Geranyl (C10) -> Farnesyl (C15) -> Squalene (C30) -> Lanosterol (C30) -> Cholesterol (C27)

mevalonate is germany’s first student loan company

note: require NADPH cofactor, ATP, Mg and Mn

179
Q

cholesterol derivatives (3 main types)

A

steroids
vitamin D
bile salts (major breakdown product of cholesterol)

180
Q

statin vs resins

A

statins inhibit hmg coa reductase (cholesterol)

resins sequesters bile acid - cholesterol complex

181
Q

what can only use glucose as metabolic source (got 2)

A

brain and NERVOUS TISSUE

* ok by right can use ketone also but like they acidic and too much will kena toxic and die

182
Q

in FH (familial hypercholesterolamia), whats the problem

A

genetic condition, cannot take up LDL cuz the LDLR spoil

183
Q

hmg-coa inhibitor or hmg-coa reductase inhibitor correct

A

REDUCTASE CHILD!! MUST HAVE THE WORD REDUCTASEEEEEE

184
Q

neural crest cells (neuroectoderm) give rise to what

A

schwann cells, sensory and autonomic ganglion, adrenal medulla, melanocytes (MAGS), retina, posterior pituitary gland

185
Q

broca’s aphasia vs wernicke;s aphasia

A

broca: broken speech, but can understand
wernicke: good speed, but cannot understand

186
Q

how many nerves and vertebrae in cervical?

A

8 nerves, 7 vertebrae

187
Q

where does spinal cord end

A

L2 at conus medullaris

continues as the cauda equina
note: lumbar puncture performed at L4/5 since spinal cord already ended.

188
Q

grey matter contain what

specify

  1. dorsal horn
  2. lateral horn
  3. ventral horn
A

cell bodies!

  1. sensory neurons
  2. autonomic neurons
  3. motor neurons
189
Q

white matter contain what

specify

  1. dorsal column/funiculus
  2. lateral column/funiculus
  3. ventral column/funiculus
A

axons and myelin sheath

  1. sensory/ascending tracts
  2. autonomic, ascending and descending tracts
  3. motor/descending tracts
190
Q

where does decussation occur

A

just before the junction between the medulla oblongata and the spinal cord

191
Q

lesion to motor pathway vs lesion to sensory pathway

  1. lesion BEFORE decussation
  2. lesion AFTER decussation

deficit where

A
  1. BEFORE
    motor - opposite
    sensory - same
  2. AFTER
    motor- same
    sensory - opposite
192
Q

somatic motor vs visceral motor

*transmit impulse where

A

somatic- skeletal muscles

visceral - smooth muscles and glands

193
Q

visceral sensory transmit what from where

A

transmit pain/subconscious visceral reflex sensation from hollow vessels, internal organs to glands to the CNS

note: visceral sensory are NOT part of ANS

194
Q

STRUCTURE OF SPINAL NERVE
dorsal root vs ventral root
dorsal ramus vs ventral ramus

A

ROOT:
dorsal - general sensory fibres to posterior horn of spinal cord
ventral - somatic motor fibres from cell bodies in spinal cord

^ these will unite to form MIXED SPINAL NERVE

RAMUS:
dorsal - supply nerve fibres to synovial joint of vertebral column, deep muscles of back and overlying skin
ventral - supply anterior and lateral trunk, upper and lower limbs

195
Q

ANS step by step

A

control centre at hypothalamus -> preganglionic fibres project form spinal cord -> synapse at autonomic ganglia -> post-ganglionic fibres emerge and from terminal networks in target tissues/organs

tldr: hypothalamus -> preganglionic -> synapse :D -> post ganglionic

196
Q

white ramus communicans vs grey ramus communicans

A

white ramus communicans
*carries preganglionic sympathetic fibers to sympathetic chain

grey ramus communicans
*carries postganglionic sympathetic fibers rejoining the spinal nerve

197
Q

referred pain

visceral afferent fibres synapse at sympathetic ganglia???

A

NO. THEY JUST CONTINUE TO SPINAL CORD THROUGH DORSAL ROOT!!!

Visceral afferent fibres run with sympathetic efferent, DO NOT SYNAPSE at sympathetic ganglia, continue to to spinal cord through DORSAL ROOT.
-Dorsal root ganglia have both somatic and visceral sensory neurones→ causes mixing up, body misperceives visceral organ pain as skin pain

198
Q

shen me shi

  • m line
  • z disc
  • a band
  • i band
  • h zone
A

M-line: attachment for thick filaments (myosin)

Z-disc: dense protein that serve as an attachment for thin filament (actin), multiple discs form a Z-line that separates sarcomeres

A band: dark bands of thick myosin filaments

I band: light bands of thin actin filaments (not covered by thick filaments)

H zone/band: region composed of only thick filaments (with no overlap with thin filaments)

199
Q

when calcium bind to troponin, what happens

A

cause tropomyosin to move, thus freeing myosin

200
Q

cross bridge cycling

A

go and look at image

201
Q

b- lymphocytes express what cd

A

cd19 and cd20

202
Q

germinal centres what happen

A

b cell can differentiate into plasma cell and memory cell

note:
SIGNAL 1 - MHCII and TCR, costimulation by B7 and CD28 (T cell activation)

SIGNAL 2 - process directed by Tfh -> provide direct co stimulation of B cell via CD40R (B cell) and CD40L (on T cell)

203
Q

somatic hypermutation vs class switching

polyclonal vs monoclonal

A
somatic hypermutation: change in VARIABLE region, increase AFFINITY of ab to antigen 
class switching: change in CONSTANT (Fc) region, change in effector function (e.g. IgM-> IgG)

polyclonal: ab from different b cell lineages able to recognise multiple different epitopes of a single antigen
monoclonal: ab clones of same parent cell, only recognise single epitope of single antigen

tldr; polyclonal = can recognise many many epitope. monoclonal = dumb fks only can recognise that one

204
Q

which Ig can cross placenta

A

IgG

205
Q

when IgA produced

A

body secretions in mucosal areas e.g. gut, respiratory tract, breast milk

note: prevent mucosal surface from colonisation by pathogens

206
Q

what composition of cell, highest survival rate for cancer

A

Th1 high, Th17 LOW

207
Q

mutant foxp3 transcription factor how

A

IPEX

note: foxp3 impt for treg

208
Q

Tcells have what CD

A

ALL HAVE CD3!!!! and CD28

note: cd28 is a receptor for CD80/86, which is needed for TCELL ACTIVATION

209
Q

cortex vs medulla (which part of thymus)

A

cortex: outer part of thymus
medulla: inner part of thymus

210
Q

3 signals of CD4+ T cell

A
  1. mhc to tcr
  2. cd80/86 to CD28
  3. specific cytokine e.g. IL-4 for Th2
211
Q

3 signals of CD4+ T cell

A
  1. mhc to tcr
  2. cd80/86 to CD28
  3. specific cytokine e.g. IL-4 for Th2
212
Q

Gs protein vs Gi protein

A

Gs ACTIVATES adenylate cyclase, therefore INCREASE cAMP production

Gi do opposite

note:
Gq activates PLC-beta, increase diacylglycerol, increase IP3, increase protein kinase c activity, increase CYTOPLASMIC CA2+
By alters ion channel function, ACTIVATES PI3K and PLC-beta

213
Q

Gq vs By

A

Gq activate PLC-beta which increase diacylglycerol, increase IP3, increase Ca2+, increase protein kinase c activity

By affect ion channel function, activate PI3K and PLC-beta

note: Gs ACTIVATES adenylate cyclase, therefore INCREASE cAMP production

214
Q

is the loss of p63 staining myoepithelial cells in ducts and lobules normal?

A

NO! myoepithelial cells (in breast) usually stain positive for p63

215
Q

superior and posterior boundary of posterior mediastinum

A

superior: transverse line from sternal angle to lower border of T4
posterior: TV to TXII

216
Q

cervical oesophagus start where

A

C6, end at jugular notch

217
Q

what level hemiazygos vein cross to the right to drain into azygous vein

A

t8/9

cross to the right BEHIND aorta, thoracic duct and oesophagus

note: vs accessory hemiazygous vein => cross at T7/8

218
Q

is accessory hemiazygous vein anterior or posterior to thoracic aorta

A

posterior

219
Q

where does the thoracic lymphatic drainage start

A

L2 from cisterna chyli!!

note: it travels on the RIGHT of thoracic aorta and oesophagus, LEFT of azygous vein

220
Q

thoracic lymphatic drainage when cross midline to left (via behind oesophagus)

A

T5

it then passes over the dome of left pleura and anterior to the left vertebral and subclavian arteries

221
Q

what goes through aortic hiatus

A

T12!! azygous vein, aorta and thoracic duct

222
Q

thoracic duct drain which one

option1: upper left body and whole body below diaphragm
option2: upper right body

A

OPTION 1: upper left body and whole body below diaphragm!!

upper right body is by right lymphatic duct

223
Q

sympathetic nerve how to enter abdomen (where)

A

pierce crus of diaphragm or by passing posterior to the medial arcuate ligament

224
Q

infectious dose vs infectivity

A

infectious dose = ability of bacterium to initiate infections

infectivity = ability of bacterium to initiate infections

therefore, lower infectious dose -> HIGHER infectivity

225
Q

what are the hall marks of cancer (10)

A
  1. growth signal autonomy
  2. evasion of growth inhibitory signal
  3. avoiding immune destruction
  4. unlimited replicative potential
  5. tumour-promoting inflammation
  6. invasion and metastasis
  7. angiogenesis
  8. genome instability and mutation
  9. evasion of cell death
  10. reprogramming energy metabolism
226
Q

dementia and cachexia what happen to the cell? (e.g. hypertrophy??)

A

atrophy (decrease SIZE of cells)

NOT NUMBER!!

227
Q

necrosis vs apotosis

  1. need ATP
  2. most common outcome
  3. inflammation?
  4. characteristics
A
  1. necrosis - NO NEED ATP, apoptosis - YES
  2. necrosis - i die, we all tie tgt (damage surrounding tissue), apoptosis - single cell death
  3. necrosis - YES INFLAMMATION, apoptosis - NO inflammation
  4. characteristics
    necrosis - irreversible plasma membrane damage with organelle breakdown
    apoptosis - condensation into apoptotic bodies -> rapid phagocytosis (membranes left intact)
228
Q

…sarcoma means what and spread by what

A

malignant mesenchymal tumour, VASCULAR spread

vs carcinoma: malignant EPITHELIAL tumour, LYMPHATIC spread

229
Q

cushing disease is waht

A

Cushing disease is a condition in which the pituitary gland releases too much adrenocorticotropic hormone (ACTH)

230
Q

HIV coreceptor is what

A

CCR5 (mostly) - macrophages, DC, Tcells
CXCR4 (mutated) - T cells

bind to GP 120

231
Q

which fungi most likely to develop after antibiotic therapy

A

candida albicans

232
Q

A patient presents with white plaques on the buccal mucosa and tongue. Upon further investigation, it is confirmed to be oral thrush, or oropharyngeal candidiasis. What is a predisposing factor?

A

antibiotic therapy

233
Q

what fungi can kena because of impaired cell-mediated immunity

A

candida (mucosal infection) and cryptococcus

234
Q

which fungi can kena cause of

  1. diabetes
  2. impaired mucosa, physical breach of epithelial barriers
  3. high dose corticosteroids (organ transplant)
  4. HIV
A
  1. candida
  2. candida
  3. aspergillus
  4. cryptococcus
235
Q

primary pathogens (4 types)

A

Coccidioides immitis
Histoplasma capsulatum
Blastomyces dermatitidis
Paracocidioides brasiliensis

236
Q

what is candida defence

A

experience starvation in phagolysosome -> germination and escape

*which is prevented by neutrophils

237
Q

aspergillus aka mold can kena from where

A

airborne and ubiquitous

note:
aspergilloma in cavity lung disease

chronic necrotising aspergillosis in chronic lung disease/mild immunocompromised

Invasive pulmonary aspergillosis in immunocompromised

Allergic bronchopulmonary aspergillosis (bronchiectasis with pulmonary consolidation) in asthma

238
Q

body defence to aspergillus

A

NETs

239
Q

cryptococcus aka yeast from where

A

soil, trees, airborne!!

ENCAPSULATED yeast most common lethal fungal infection in pt with AIDS worldwide

240
Q

how body defend against cryptococcus

A

use alveolar macrophages and cd4 th1 response to clear

*usually fungi would multiply in macrophage phagosome and after that escape

241
Q

antifungal drugs do what

  1. azole, polyene, allylamines
  2. pyrimidine analogues
  3. echinocandins
A
  1. ergosterol (cell membrane of fungi)
  2. dna synthesis
  3. cell wall (chitin and glucans)
    * non-specific inhibition of b-1,3 glucan synthase
242
Q

NK cell for what type of infection? viral fungal or bacteria

A

VIRAL

243
Q

Fever, bloody diarrhoea (dysentery), abdominal pain, liver abscess . symptoms of what

esp if trophozoites with endocytosed RBCs

A

entamoeba histolytica

244
Q

taenia spp. (cestode) what type in pig in beef

A

pig: t. solium
* cause cysticercosis (EPILEPSY)
beef: t. saginata

245
Q

plasmodium spp.

  1. nucleus look like what
  2. can cause what
A

head phone, ring shaped
cause malaria: fever, headache, anaemia, splenomegaly

Falciparum malaria - infected RBCs stick to capillary walls, blocking them, thus leading to ischaemia of brain, kidney, lungs

246
Q

what cause intermittent/spiking fever, pancytopenia, hepatosplenomegaly, Kala-azar (black fever - skin hyperpigmentation), weight loss,

skin lesions and disfiguring ulceration

A

leishmania spp. (got tail, look like sperm but the head look like beauty blender)

247
Q

bloatedness, flatulence, steatorrhea caused y what

A

giardia lamblia (look like face)

248
Q

burning, itching of inflamed cervix (which appears erythematous with petechiae), frothy, yellow-green, foul-smelling discharge

A

Trichomonas vaginalis (motile pear-shaped trophozoites)

249
Q

diarrhoea and malabsorption

A

Strongyloidiasis

nematode

250
Q

Cause schistosomiasis - hepatosplenomegaly, liver cirrhosis and fibrosis, portal hypertension

lead to squamous cell carcinoma of the bladder and pulmonary hypertension

what is it

A

Schistosoma spp. (trematode)

251
Q

pathway of temperature signal

A

temperature (sensor in skin) -> AFferent signal into spinal cord via Lissauer’s tract -> passed to LATERAL spinothalamic tract -> hypothalamus (pre-optic area, dorsal hypothalamus) -> central heat receptors in hypothalamus -> signal to tissue for homeostasis

252
Q

what can cause saddle back fever

A

dengue, leptospirosis, legionnaire’s disease

253
Q

what can cause spiking fever

A

TB, abscess, schistosomiasiss

254
Q

what cause remitting fever

A

amoebiasis, malaria, kawasaki disease

255
Q

what cause longer periodicity fever

A

pel-ebstein fever from lymphoma

256
Q

A 33-year-old patient is suffering from a sudden occlusion at the origin of the descending (thoracic) aorta.
This condition would most likely decrease blood flow in which of the following intercostal arteries?

A

lower nine posterior

ICS 3-11

first 2 is by costocervical trunk

257
Q

aortic hiatus what arcuate ligament

A

MEDIAN

258
Q

alveolar dead space why

A

not enough BLOOD SUPPLY

259
Q

requirements for effective airflow

A

Alveoli open
Airways patent
Pleural layers sliding easily.

260
Q

airway vs respiratory units (NORMAL)

A

airway: 70% macrophages, 30% neutrophil
respiratory: 90% macrophages, 10% neutrophil

note: COPD 30% macrophage, 70% neutrophil

261
Q

pulmonary oedema -> restrictive or obstructive?

A

RESTRICTIVEEEEEE, will decrease lung compliance

poor left ventricular function → excess blood in pulmonary vasculature → vascular engorgement, extravasation due to increased hydrostatic pressure and pulmonary oedema → makes lung stiffer and reduce compliance

262
Q

MEN2 caus what tumour

A

thyroid gland, adrenal gland, and parathyroid glands.

263
Q

which MMR (mismatch repair) genes work cooperatively

for DNA

A

MLH1 + PMS2

MLH2 + MSH6

264
Q

what is MSI (microsatellite instability)

A

repeated DNA motifs, usually in non-coding DNA

265
Q

lynch syndrome aka HNPCC ( Hereditary Non-Polyposis Colon Cancer)

A

Caused by mutations in MMR genes, especially MLH1, MSH2, and MSH6, which leads to microsatellite instability

Patients develop colorectal and endometrial cancer

Autosomal dominant inheritance

266
Q

how to treat breast cancer (mutation in BRCA1 and BRCA2)

A

PARP inhibitor

267
Q

steps of metastasis (5 steps)

A
  1. invasion (EMT)
  2. intravasation (tumour cell enter blood stream, transendothelial migration)
  3. transport/dissemination (sheer stress survival)
  4. extravasation (transendothelial migration)
  5. metastatic colonization
268
Q

EMT transcription factor upregulate/downregulate what shits

A

upregulate N-cad and MMPs

downregulate E-cad

269
Q

Dyskeratosis congenita (DC) caused by what

A

mutation in telomerase or telomere binding sheltering complex

!!=> premature aging and stem cell failure

270
Q

p53 regulated by what ubiquitin ligase

A

MDM2

271
Q

WHATS THAT SOUND?

radiate to carotids, late DIASTOLIC murmur (s3)

A

aortic REGURGITATION

diastolic -> aortic regu or mitral stenosis

mitral: mid-diastolic murmur

272
Q

WHATS THAT SOUND

systolic murmur + radiate to carotids

A

aortic stenosis since SYSTOLIC + carotids

systolic -> aortic stenosis/ mitral regur